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dc.contributor.authorGuoli Wang
dc.contributor.authorTianyue An
dc.contributor.authorCong Lei
dc.contributor.authorXiaofeng Zhu
dc.contributor.authorLi Yang
dc.contributor.authorLianxue Zhang
dc.contributor.authorRonghua Zhang
dc.contributor.otherCollege of Pharmacy, Jinan University, Guangzhou, China
dc.contributor.otherCollege of Pharmacy, Jinan University, Guangzhou, China
dc.contributor.otherCollege of Pharmacy, Jinan University, Guangzhou, China
dc.contributor.otherCollege of Traditional Chinese Medicine, Jinan University, Guangzhou, China; Department of the First Affiliated Hospital, Jinan University, Guangzhou, China
dc.contributor.otherCollege of Pharmacy, Jinan University, Guangzhou, China
dc.contributor.otherCollege of Chinese Medicinal Materials, Jilin Agricultural University, Changchun, China; Corresponding author. College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun, 130118, China.
dc.contributor.otherCollege of Pharmacy, Jinan University, Guangzhou, China; Corresponding author. College of Pharmacy, Jinan University, Guangzhou, 510632, China.
dc.date.accessioned2022-05-11T04:20:01Z
dc.date.available2025-10-02T05:35:01Z
dc.date.issued01-05-2022
dc.identifier.issn-
dc.identifier.urihttp://www.sciencedirect.com/science/article/pii/S1226845321000385
dc.description.abstractBackground: Brain-derived neurotrophic factor (BDNF)–tropomyosin-related kinase B (TrkB) plays a critical role in the pathogenesis of depression by modulating synaptic structural remodeling and functional transmission. Previously, we have demonstrated that the ginsenoside Rb1 (Rb1) presents a novel antidepressant-like effect via BDNF–TrkB signaling in the hippocampus of chronic unpredictable mild stress (CUMS)-exposed mice. However, the underlying mechanism through which Rb1 counteracts stress-induced aberrant hippocampal synaptic plasticity via BDNF–TrkB signaling remains elusive. Methods: We focused on hippocampal microRNAs (miRNAs) that could directly bind to BDNF and are regulated by Rb1 to explore the possible synaptic plasticity-dependent mechanism of Rb1, which affords protection against CUMS-induced depression-like effects. Results: Herein, we observed that brain-specific miRNA-134 (miR-134) could directly bind to BDNF 3′UTR and was markedly downregulated by Rb1 in the hippocampus of CUMS-exposed mice. Furthermore, the hippocampus–targeted miR-134 overexpression substantially blocked the antidepressant-like effects of Rb1 during behavioral tests, attenuating the effects on neuronal nuclei-immunoreactive neurons, the density of dendritic spines, synaptic ultrastructure, long-term potentiation, and expression of synapse-associated proteins and BDNF–TrkB signaling proteins in the hippocampus of CUMS-exposed mice. Conclusion: These data provide strong evidence that Rb1 rescued CUMS-induced depression-like effects by modulating hippocampal synaptic plasticity via the miR-134-mediated BDNF signaling pathway.
dc.format-
dc.language.isoEN
dc.publisherElsevier
dc.relation.uri['http://journal.unsika.ac.id/index.php/jurnalilmiahhukumdejure', 'http://journal.unsika.ac.id/index.php/jurnalilmiahhukumdejure/about/submissions#authorGuidelines', 'http://journal.unsika.ac.id/index.php/jurnalilmiahhukumdejure/about/editorialPolicies#focusAndScope']
dc.rightsCC BY
dc.subject['constitutional law', 'law', 'criminal law', 'civil law', 'law enforcement', 'regulation', 'Law', 'K', 'Law in general. Comparative and uniform law. Jurisprudence', 'K1-7720']
dc.subject.lccBotany
dc.titleAntidepressant-like effect of ginsenoside Rb1 on potentiating synaptic plasticity via the miR-134–mediated BDNF signaling pathway in a mouse model of chronic stress-induced depression
dc.typeArticle
dc.description.keywordsGinsenoside Rb1
dc.description.keywordsDepression
dc.description.keywordsmiR-134
dc.description.keywordsBDNF–TrkB signaling
dc.description.keywordsSynaptic plasticity
dc.description.pages376-386
dc.description.doi10.1016/j.jgr.2021.03.005
dc.title.journalJournal of Ginseng Research
dc.identifier.e-issn-
dc.identifier.oaioai:doaj.org/journal:113a4d4f34b24b59a0488a3d4f54f1c5
dc.journal.infoVolume 46, Issue 3


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